Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.6 (RNA polymerase)
 34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although not thought to become competent for DNA uptake, the bacterium Streptococcus pyogenes appears to encode within its genome the DNA uptake and recombination machinery required for competence. The promoters of these genes contain a conserved sequence, CIN-box, which is recognized by the S. pyogenes alternative RNA polymerase sigma factor X. Using microarray technology, we found that sigma X induced the expression of competence genes in S. pyogenes. Real-time RT-PCR was performed to confirm that the expression of these transcripts was induced 2-265-fold by sigma X. Of the eight CIN-box loci induced, femB, the ortholog a virulence factor in Staphylococcus aureus, was shown to be transcribed in vitro by RNA polymerase containing sigma X, indicating that sigma X directly activates expression of this CIN-box gene. Sigma X-dependent induction of genes encoding competence machinery in S. pyogenes raises the possibility that some strains of this human pathogen can develop competence for genetic transformation.
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PMID:Sigma X induces competence gene expression in Streptococcus pyogenes. 1696 31

Horizontal gene transfer is an important means of bacterial evolution. This includes natural genetic transformation, where bacterial cells become "competent" and DNA is acquired from the extracellular environment. Natural competence in many species of Streptococcus, is regulated by quorum sensing via the ComRS receptor-signal pair. The ComR-XIP (mature ComS peptide) complex induces expression of the alternative sigma factor SigX, which targets RNA polymerase to CIN-box promoters to activate genes involved in DNA uptake and recombination. In addition, the widely distributed Streptococcus prophage gene paratox (prx) also contains a CIN-box, and here we demonstrate it to be transcriptionally activated by XIP. In vitro experiments demonstrate that Prx binds ComR directly and prevents the ComR-XIP complex from interacting with DNA. Mutations of prx in vivo caused increased expression of the late competence gene ssb when induced with XIP as compared to wild-type, and Prx orthologues are able to inhibit ComR activation by XIP in a reporter strain which lacks an endogenous prx. Additionally, an X-ray crystal structure of Prx reveals a unique fold that implies a novel molecular mechanism to inhibit ComR. Overall, our results suggest Prx functions to inhibit the acquisition of new DNA by Streptococcus.
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PMID:The conserved mosaic prophage protein paratox inhibits the natural competence regulator ComR in Streptococcus. 3040 83